[Neutrophils' contribution to ischaemia and reperfusion injury in liver]. / Udzial neutrofili w uszkodzeniu watroby na skutek niedokrwienia i reperfuzji.

Neutrophils are cells which induce liver injury due to ischaemia and reperfusion. They are active especially in the later phase of reperfusion (> 6 hrs) since they gather in the liver and release mediators damaging hepatocytes directly. Inflow ofneutrophils into the liver is possible due to chemotaxia which involves, among others, chemokines CXC (interleukin-8 and its counterparts). Neutrophils' ability to induce chemotaxia is determined by their specific glycoprotein receptors in cell membranes. Neutrophils contribute to ischaemia/reperfusion liver injury because they adhere to vessel endothelium, cross the wall of hepatic microcirculation vessels and adhere to hepatocytes. Selectins play a crucial role in neutrophils' contact with endothelial cells, and ICAM-1, predominantly in their adhesion to hepatocytes. Also beta2-integrin and Mac-1 play essential role. Neutrophils damage hepatocytes by realising proteases, free radicals, TNF-alpha, TGF-beta and leucotrien. Neutrophils together with endothelial cells also disturb the hepatic microcirculation.

[Apoptosis and necrosis--two different ways leading to the same target]. / Apoptoza i martwica--dwie drogi do jednego celu.

Both apoptosis and necrosis lead to the same target, i.e. the death of the cell. However their mechanisms are different although they are evoked by similar factors. The differences between apoptosis and necrosis concern not only morphological features but also biochemical changes taking place in the cell. In the case of apoptotic death of cell, its intracellular content is not released and that is why inflammatory reaction, which is present in necrosis, is absent. In necrosis, defined as a passive death, majority of enzymes as well as metabolic tracts are lost and the released lysosome enzymes digest cellular components. Apoptosis, on the other hand, is an active process which requires supply of adenosine triphosphate (ATP) and which is controlled by many genes. There are many factors that determine the kind of cell death. The most important of them seems to be the level of intracellular ATP connected with caspase activation. This is the reason why mitochondria are considered to be the main cell organelles, which determine the type of cell death. Disturbances in the flow of ions connected with the activation of specific ion channels as well as free oxygen radicals are of importance here, too.

[Therapeutic management of hepatic encephalopathy]. / Postepowanie terapeutyczne w encefalopatii watrobowej.

Therapeutic management in hepatic encephalopathy depends on its etiology as well as progression degree. Both in acute and chronic encephalopathy one should tend to establish probable causes and try to eliminate them. Cutting down on proteins in diet is one of the most important suggestions in chronic hepatic encephalopathy. In order to reduce intestinal production of ammonia, non-absorbable disaccharides (lactulose), antibiotics (neomycin) and sodium benzoate are the most commonly used. Branched chain amino acids administered orally or parenterally may be useful in improving patient's condition and restoring the balance of blood amino acids. The GABA-benzodiazepine receptor theory led to application of its antagonists, such as flumazenil, in the management of hepatic encephalopathy. However, providing a proper treatment is not easy due to unstable and often not very characteristic course of hepatic encephalopathy. What is more, clinical trials of some drugs used in the treatment of hepatic encephalopathy do not confirm their effectiveness.